RT Journal Article
SR Electronic
T1 Proinflammatory and autoimmunogenic gut microbiome in systemic lupus erythematosus
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 621995
DO 10.1101/621995
A1 Chen, Bei-di
A1 Jia, Xin-miao
A1 Xu, Jia-yue
A1 Zhao, Li-dan
A1 Ji, Jun-yi
A1 Wu, Bing-xuan
A1 Fei, Yun-yun
A1 Yang, Hua-xia
A1 Chen, Hua
A1 Zuo, Xiao-xia
A1 Li, Hui
A1 Pan, Wen-you
A1 Wang, Xiao-han
A1 Ye, Shuang
A1 Guo, Dong-geng
A1 Wang, Li
A1 Li, Jing
A1 Peng, Lin-yi
A1 Zheng, Wen-jie
A1 Zhang, Wen
A1 Zhang, Feng-chun
A1 Zhang, Jian-min
A1 He, Wei
A1 Cao, Xue-tao
A1 Liu, De-pei
A1 Wang, Jun
A1 Zhang, Xuan
YR 2019
UL http://biorxiv.org/content/early/2019/04/29/621995.abstract
AB Systemic lupus erythematosus (SLE), characterized by chronic inflammation and multi-organ damage, has been suggested to associate with gut dysbiosis, but knowledge is limited from small sample size and 16s rRNA-based studies. To shed new light on the role of microbiota in SLE development, we analyzed the fecal metagenome of 117 treatment-naïve SLE patients and 115 sex- and age-matched healthy controls (HC) by deep-sequencing; in addition, 52 of the aforementioned patients have post-treatment fecal metagenome for comparison. We found significant differences in microbial composition and function between SLE and HC, revealing multiple plausible contributing bacterial species and metabolic pathways in SLE. In-depth SNP-based analysis revealed an oral-microbiome origin for two marker species, strengthening the importance of bacterial translocation in disease development. Lastly, we confirmed experimentally that peptides of SLE-enriched species mimicking autoantigens such as Sm and Fas could trigger autoimmune responses, suggesting a potential causal role of gut microbiota in SLE.